Trauma depresses the natural host defense mechanisms and this depression renders a patient susceptible to infection. The increased incidence and severity of sepsis in trauma-depressed patients is a leading cause of mortality and is influenced only slightly by antibiotic therapy. While the exact nature and extent of the impairment of host resistance has not yet been fully clarified, it is generally agreed upon that suppression of specific immune function, and particularly of cell-mediated immune function, is one of the most dramatic and consistent failures in the host defenses following trauma. Recent findings in this laboratory indicate that burn-traumatized, immunodepressed experimental animals show evidence of increase suppressor cell activity in spleen cell population. This finding may provide the first clue to the underlying causes of immune aberations in traumatized subjects. We propose to investigate the phenomenon of trauma-induced suppressor cells in order to determine the nature and characteristics of these cells and to determine if trauma induces changes in the activities of other lymphocyte subpopulations. We also intend to study the factors and events subsequent to trauma which contribute to the generation of suppressor cells. We further intend to investigate the effects of immunoenhancing adjuvants on the activity of suppressor and helper subpopulations to determine if such agents can alter the depressed immune state in traumatized subjects. By such studies we can achieve a better understanding of trauma-induced immunodepression and we can begin to devise approaches to a more rational therapy in trauma patients.